(Hypertension. 2002;39:214.)
© 2002 American Heart Association, Inc.
Scientific Contributions |
From the Vascular Biology and Hypertension Program of the Department of Medicine, University of Alabama at Birmingham.
Correspondence to J. Michael Wyss, PhD, Department of Cell Biology, 1670 University Blvd, Birmingham, AL 35294-0019. E-mail jmwyss{at}uab.edu
ACE plays an important role in the regulation of arterial pressure; however, a linear relationship between ACE expression and arterial pressure has not been demonstrated. The present study employed telemetric monitoring in female transgenic mice to determine the influence of partial and complete deletion of the ACE gene on basal arterial pressure and arterial pressure responses to a high-NaCl diet. On the basal NaCl diet, 24-hour mean arterial pressure was significantly correlated with the number of functional copies of the ACE gene; ie, arterial pressure was lowest in 0-copy (80±1 mm Hg), intermediate in 1-copy (100±1 mm Hg), and highest in 2-copy (113±1 mm Hg) ACE mice. The high-NaCl diet significantly increased mean arterial pressure in 0-copy (99±1 mm Hg) and 1-copy (108±1 mm Hg) mice but not in 2-copy mice (114±1 mm Hg). These results demonstrate a copy-dependent relationship between ACE gene expression and both basal arterial pressure and arterial pressure responses to a high-NaCl diet, suggesting that either partial or complete reduction in the ACE gene can alter arterial pressure.
Key Words: angiotensin-converting enzyme arterial pressure renin-angiotensin system sodium
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